Diabetology & Metabolic Syndrome最新文献

Background: Both the triglyceride-glucose (TyG) index, a predictor of insulin resistance (IR), and inflammation are risk factors for stroke in hypertensive patients. However, only a handful of studies have coupled the TyG index and inflammation indices to predict stroke risk in hypertensive patients. The C-reactive protein-triglyceride-glucose index (CTI) is a novel marker that comprehensively assesses the severity of IR and inflammation. The present study explored the association between CTI and the risk of stroke in patients with hypertension.

Methods: A total of 3,834 hypertensive patients without a history of stroke at baseline were recruited from the China Health and Retirement Longitudinal Study (CHARLS). Multivariate Cox regression and restricted cubic spline (RCS) analyses were employed to assess the relationship between CTI and stroke risk in hypertensive patients. Furthermore, the Boruta algorithm was applied to evaluate the importance of CTI and construct prediction models to forecast the incidence of stroke in the study cohort.

Results: After 7 years of follow-up, the incidence of stroke in hypertensive patients was 9.6% (368 cases). Multivariate Cox regression analysis revealed a 21% increase in stroke risk with an increase in each CTI unit (hazard ratio (HR) = 1.21, 95% confidence interval (CI) = 1.08-1.37). The top quartile group was 66% more likely to have a stroke than the bottom quartile group (HR = 1.66, 95% CI = 1.23-2.25). RCS analysis confirmed a linear relationship between CTI and stroke risk. The Boruta algorithm validated CTI as a crucial indicator of stroke risk. The Support Vector Machine (SVM) survival model exhibited the best predictive performance for stroke risk in hypertensive patients, with an area under the curve (AUC) of 0.956.

Conclusions: An increase in CTI levels is associated with a higher risk of stroke in hypertensive patients. This study suggests that CTI may emerge as a unique predictive marker for stroke risk.

Background: Proximal renal tubular dysfunction occurs during diabetic ketoacidosis (DKA) in type 1 diabetes. However, only a few studies have reported on the multiple proximal renal tubular functions simultaneously. Moreover, to the best of our knowledge, distal renal tubular function has not yet been investigated.

Methods: Patients with newly diagnosed type 1 diabetes mellitus were classified into those with DKA and those without DKA, and their proximal and distal renal tubular functions were investigated. The diagnostic criteria for DKA were blood glucose > 200 mg/dL, blood pH < 7.3 or HCO₃^- < 15 mEq/L, and urine ketone body positivity.

Results: Six patients with DKA and five patients without DKA were included. In patients with DKA, urinary β2-microglobulin levels were significantly higher, while blood pH, HCO₃^-, and tubular reabsorption of phosphorus were significantly lower than in those without DKA. There were no significant differences in blood glucose, HbA1c, serum phosphorus, urinary N-acetyl-beta-glucosaminidase, and urinary amino acid excretion between patients with and without DKA. Elevated NH₃ levels and impaired urinary acidification were not observed in patients with and without DKA.

Conclusions: In patients with newly diagnosed type 1 diabetes mellitus complicated with DKA, multiple proximal renal tubular dysfunctions occur simultaneously, suggesting transient Fanconi syndrome. Distal renal tubular acidosis was unlikely. The diagnostic criteria for DKA are appropriate also in the view of proximal renal tubular dysfunction and are considered suggestive of pathophysiological factors that may cause proximal renal tubular dysfunction.

Introduction: Diabetic cardiomyopathy (DCM) is a significant complication of diabetes, characterized primarily by the development of heart failure in individuals with diabetes. Numerous animal studies have indicated that resveratrol enhances cardiac function in diabetic cardiomyopathy; however, its reliability and underlying mechanism remain unclear. This study aims to assess the cardioprotective effects of resveratrol on DCM and explore its potential mechanism.

Methods: We searched PubMed, EMBASE, WOS, Cochrane Library, CNKI, CBM, Chinese VIP, and Wan Fang Database until March 31st, 2024, without language restrictions. Continuous outcome measures were analyzed using weighted mean difference or standardized mean difference, and heterogeneity was assessed with I². The risk of bias in animal experiments was evaluated using the SYRCLE tool, and evidence reliability was determined with the GRADE tool. All data were analyzed using Review Manager 5.4.1 and Stata 17. This study has been registered on the PROSPERO (CRD42024523944).

Results: A total of 18 studies meeting the criteria were identified. The analysis revealed that the resveratrol intervention group exhibited significant improvements in LVEF (WMD = 17.88), LVFS (WMD = 8.77), HW/BW (SMD=-2.92), SOD (SMD = 4.53), and MDA (SMD=-5.07) compared to the control group. The GRADE grading assessment indicated moderate certainty for LVEF, HW/BW, and MDA, while certainty for other factors was considered low.

Conclusion: Our research suggests that resveratrol may protect cardiac function in DCM through anti-inflammatory and anti-oxidative stress effects. However, these findings are based on preclinical data, and further extensive trials are needed to confirm their effectiveness and safety before clinical application.

Objective: The relationship between blood glucose levels and osteoarthritis (OA) is unclear. This study aimed to investigate the genetic causal relationship between blood glucose-related traits and OA.

Methods: We first performed univariate Mendelian randomization (UVMR) analyses using published genome-wide association study (GWAS) datasets with fasting glucose (FG), 2 h-glucose post-challenge glucose (2hGlu), and glycosylated hemoglobin (HbA1c) as exposures, and hip osteoarthritis (HOA) and knee osteoarthritis (KOA) as outcomes; then, we performed inverse analyses of them. We used Inverse-variance weighted (IVW) analysis as the primary analysis, and sensitivity analyses were performed. Moreover, we performed multivariate Mendelian randomization (MVMR) to estimate the independent effect of exposure on outcome after adjusting for body mass index (BMI). Summarized data for blood glucose-related traits were obtained from the MAGIC Consortium study of the glucose trait genome and for OA from the UK Biobank and arcOGEN. Summarized data for BMI were obtained from the GIANT Consortium meta-analysis of individuals of European ancestry. A two-sided p value < 0.05 in UVMR was considered suggestive of significance when p < 0.0167 (Bonferroni correction p = 0.05/3 exposures) was considered statistically significant.

Results: We found significant negative genetic causality of FG for HOA and KOA, and these associations remained significant after we adjusted for the effect of BMI [odds ratios (ORs) of 0.829 (0.687-0.999, p = 0.049) and 0.741 (0.570-0.964, p = 0.025)]. HbA1c also had an independent negative genetic causal effect on HOA after adjustment for BMI [0.665 (0.463-0.954, p = 0.027)]. At the same time, there was no evidence of reverse genetic causality of OA on blood glucose-related traits.

Conclusion: We further elucidated the relationship between blood glucose-related traits and OA by adjusting for the effect of BMI from a genetic causal perspective. This study provides new insights to further clarify the relationship between blood glucose levels and OA, as well as the pathogenesis, etiology and genetics of OA.

Objective: Type 2 diabetes mellitus (T2DM) poses a substantial global health concern. Statins are widely used among T2DM patients for managing dyslipidemia, preventing cardiovascular disease (CVD), and offering renal protection. However, the extent to which their renal protective effects contribute to reducing the incidence of severe renal complications, including chronic kidney disease (CKD) and renal failure, is not well-defined.

Methods: This investigation scrutinizes the impact of simvastatin versus placebo on renal outcomes among T2DM patients utilizing data from the ACCORD trial. It encompasses incidence rate comparisons, Kaplan-Meier estimates, Cox proportional hazards models, and mediation analyses.

Results: The study consisted of 3,619 individuals diagnosed with T2DM, among which 2,753 were treated routinely with simvastatin, while 866 did not receive any statin therapy. After adjusting for baseline characteristics and time-dependent covariates, simvastatin treatment was associated with a 71% reduction in the risk of CKD (HR 0.29, 95% CI 0.27-0.31, p < 0.01) and a 47% reduction in the risk of renal failure (HR 0.53, 95% CI 0.44-0.65, p < 0.01) compared to the statin-free group. Further subgroup analysis, accounting for the initial lipid and kidney profiles, indicated variable impacts of simvastatin on CKD and renal failure outcomes. Nevertheless, a consistent reduction in CKD risk was observed across all subgroups within the statin-treated population. Additional mediation analysis revealed that the reduction in low-density lipoprotein cholesterol (LDL-C) may be a potential mediator in the association between simvastatin and CKD, with a mediation effect of 14.9%, (95% CI 0.11-0.19, p < 0.01).

Conclusion: Administering statins, specifically simvastatin, to T2DM patients at elevated risk for CVD, is likely to offer augmented renal advantages, notably in lowering the occurrence of CKD and renal failure. This protective effect against CKD manifests regardless of initial lipid profiles, albuminuria, and estimated glomerular filtration rate (eGFR) levels. The association between simvastatin and CKD may be partially mediated by LDL-C reduction.

Background: Gestational diabetes mellitus (GDM) and insulin resistance (IR) increase the risk of adverse pregnancy outcomes. We aimed to examine the relationship of interstitial glucose assessed by continuous glucose monitoring (CGM) at early gestation, and the subsequent development of IR and GDM, and to determine 24-h interstitial glucose centile distributions in women with normal (non-IR and non-GDM) and suboptimal glycemic status (IR and/or GDM).

Methods: CGM measurements were taken for 3-10 days at 18-24 weeks' gestation, followed by fasting serum insulin and oral glucose tolerance testing at 24-28 weeks' gestation. IR and GDM were determined by the updated Homeostasis Model Assessment of IR score of ≥ 1.22 and 2013 World Health Organization criteria, respectively. Risks of IR and GDM were estimated using modified Poisson models, and hourly interstitial glucose centiles determined using Generalized Additive Models for Location, Scale and Shape.

Results: This prospective cohort study involved 167 pregnant women in Singapore, with a mean age of 31.7 years, body mass index of 22.9 kg/m², and gestation of 20.3 weeks. 25% of women exhibited IR and 18% developed GDM. After confounders adjustment, women with suboptimal glycemic control, indicated by higher mean daily glucose (risk ratio 1.42; 95% confidence interval 1.16, 1.73), glucose management indicator (1.08; 1.03, 1.12), and J-index (1.04; 1.02, 1.06), as well as those with greater glycemic variability, indicated by higher standard deviation (1.69; 1.37, 2.09), coefficient of variation (1.03; 1.00, 1.06), and mean amplitude of glycemic excursions (1.4; 1.14, 1.35) derived from CGM in early gestation were associated with higher risks of developing IR in later gestation. These associations were similarly observed for the development of GDM. Centile curves showed that, compared to those with normal glycemic status, women with suboptimal glycemic status had higher glucose levels, with greater fluctuations throughout 24 h.

Conclusions: In pregnant women who subsequently developed IR and GDM, interstitial glucose levels assessed by CGM were elevated and varied greatly. This supports the potential use of CGM to screen for glycemic changes early in pregnancy.

Objectives: We conducted this meta-analysis of randomized controlled trials (RCTs) to compare the efficacy of adding metformin to lifestyle interventions versus lifestyle interventions alone in individuals with prediabetes.

Materials and methods: We searched four databases from inception until March 20, 2024. Our primary outcomes included the incidence of type 2 diabetes, hemoglobin A1c (HbA1c), and fasting plasma glucose (FPG). Secondary outcomes included blood pressure, plasma lipids, and weight measurements. Dichotomous outcomes were pooled as the risk ratio (RR) and its 95% confidence interval (CI), while continuous outcomes were pooled as the standardized mean difference (SMD) and its 95% CI in the random effect model. All statistical analyses were conducted using the "meta" package of RStudio software.

Results: We included 12 RCTs, comprising 2720 patients. Adding metformin to lifestyle interventions significantly reduced HbA1c levels (SMD = -0.10, 95% CI [-0.19, -0.01], P = 0.03) and the incidence of type 2 diabetes (RR = 0.85, 95% CI [0.75, 0.97], P = 0.01). Interestingly, adding metformin to lifestyle interventions was comparable to lifestyle interventions alone in terms of FPG at both 3 and 6 months; however, it significantly reduced FPG at 12 months (SMD = -0.34, 95% CI [-0.59, -0.08], P = 0.01). There were no significant differences between the two groups in terms of all secondary outcomes.

Conclusions: Our findings suggest that adding metformin to lifestyle interventions may improve glycemic control in individuals with prediabetes and reduce their risk of progression to diabetes, compared to lifestyle interventions alone. A longer duration of this combined approach may be required to observe the desired effects.

Background: The diabetic foot (DF) ulcer is the severe complication of type 2 diabetes mellitus (T2DM). Sarcopenia is characterized as the loss of muscle mass and strength, resulting in the increased risk of fracture and physical disability. Sarcopenia may affect the foot-ankle function in DF ulcer patients, compromise the quality of life.

Objective: The aim was to clarify the effect of sarcopenia on foot-ankle function in patients with DF ulcer.

Methods: In total of 108 T2DM patients with DF ulcer were enrolled. Based on the examination of muscle mass by dual energy X-ray absorptiometry (DXA) and grip strength and 5x sit-to-stand test, the DF patients were divided into sarcopenia and non-sarcopenia groups. The severity of DF ulcer was evaluated by Wagner classification. The foot-ankle function was evaluated by American Orthopaedic Foot and Ankle Society (AOFAS) Ankle-Hindfoot Score.

Results: DF patients with sarcopenia showed advanced age, lower BMI, longer duration of T2DM, and more severe Wagner classification, reduced appendicular skeletal muscle mass index (ASMI), grip strength, transcutaneous oxygenpressure (TcPO₂) and prolonged time of 5X sit-to-stand test. The stratified comparison analysis indicated that severity of sarcopenia and DF ulcer, reduced TcPO₂, and grip strength were aggravated with the impaired foot-ankle function (P < 0.05). Multivariate Logistic analysis showed that age, TcPO₂, and severe sarcopenia were risk factors deteriorating the foot-ankle function.

Conclusion: The sarcopenia is a key risk factor of decreasing foot-ankle function in patients with DF ulcer. Thus, the prevention of muscle mass and strength loss could be considered as part of comprehensive therapy for DF ulcer.

Introduction: Type 1 Diabetes Mellitus (DM1) affects a small percentage of the population. Nevertheless, its prevalence is currently growing with alarming data on uncontrolled cases. The importance of body composition and Phase Angle (PA), assessed by Bioelectrical Impedance (BIA), in long- term DM1 patients lies in the fact that alterations in cellular integrity and body compartments may affect risk profiles and metabolic control. The objective of this study was to compare PA and body composition parameters between adults with DM1 and healthy controls.

Methods: A comparative study was carried out in a public university outpatient clinic including a cohort of adult patients of both sexes diagnosed with DM1 and healthy controls matched by age and sex in a 2:1 ratio. Anthropometric measurements included weight, height and BMI. Using the raw BIA data of Resistance and Reactance, fat-free mass (FFM), fat mass (FM), fat-free mass index (FFMI), fat mass index (FMI), PA and standardized PA (SPA) were calculated. Means or medians were compared between the groups. Regression models were used to identify distinguishing characteristics of the groups and associations within the DM1 group (i.e. glycated hemoglobin (HbA1c), disease duration, presence of microvascular complications, capillary blood glucose, BMI and FMI).

Results: 88 patients with DM1and 46 healthy controls were evaluated. PA (6.05 vs. 6.85, p = 0.000) and SPA (-1.47 vs. -0,37, p = 0.000) were lower in patients with DM1 compared to healthy controls. People with DM1 displayed higher adiposity (%FM = 29.6 vs. 27.6, p = 0.016; FMI = 7.00 vs. 6.33, p = 0.016) and lower %FFM compared to healthy controls. Most of the differences were maintained after sex stratification; however, men with DM1 showed a lower FFMI than male controls (18.2 vs. 20.16, p = 0.029).

Conclusion: Patients with DM1 present lower PA than healthy controls, which may be related to worse cell membrane integrity. Significant body composition differences between the groups and between sexes were identified, with data showing greater adiposity in women with DM1 and men displaying lower muscle mass. These findings suggest the importance of including PA and body composition evaluations in the follow-up of patients with DM1. The ultimate goal is to obtain a better metabolic control and, consequently, a better prognosis.

Background: In recent years, there has been a surge of interest in the metabolic phenotype among children with obesity characterized by the absence of associated cardiometabolic risk factors (CRFs), known as metabolically healthy obesity (MHO), as opposed to those with metabolically unhealthy obesity (MUO). This study investigated the effect of lifestyle intervention on CRFs among children with MHO and MUO.

Methods: A total of 102 school-aged children with obesity (54 girls and 48 boys) aged 8-16 years completed a 16-week school-based lifestyle modification intervention program, MyBFF@school Phase I. The intervention consisted of physical activity, healthy eating promotion, and psychological empowerment. MHO and MUO statuses were defined based on the 2018 consensus-based criteria. Fasting venous blood collection, body composition measurement, clinical assessment and physical fitness testing were conducted at baseline and at the end of week 16.

Results: After the intervention, the CRFs of the children with MUO improved with significant decreases in systolic (p < 0.001) and diastolic (p = 0.01) blood pressure and a significant increase in high-density lipoprotein cholesterol (HDL-C) (p = 0.005), while the CRFs of the children with MHO had a significant decrease in uric acid (p = 0.04). Additionally, 51.6% of the children with MHO transitioned to the MUO, while 26.8% of the children with MUO crossed over to the MHO at the end of the intervention. Furthermore, the odds of having high systolic blood pressure among children with MUO were 59% lower at week-16 than at baseline (OR = 0.41 (95% CI = 0.18, 0.92), p = 0.03).

Conclusions: Our findings demonstrated that CRFs improved more prominently among children with MUO following the intervention. More importantly, our findings indicate that MHO in children is transient, hence, strategies to protect children against MUO are warranted.

Trial registration: ClinicalTrials.gov NCT02212873.